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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

Death inducer-obliterator 1

DIO-1, DIDO1, Dido3, death inducer-obliterator 1, death-associated transcription factor 1, DATF1
Apoptosis, a major form of cell death, is an efficient mechanism for eliminating unwanted cells and is of central importance for development and homeostasis in metazoan animals. In mice, the death inducer-obliterator-1 gene is upregulated by apoptotic signals and encodes a cytoplasmic protein that translocates to the nucleus upon apoptotic signal activation. When overexpressed, the mouse protein induced apoptosis in cell lines growing in vitro. This gene is similar to the mouse gene and therefore is thought to be involved in apoptosis. Alternatively spliced transcripts have been found for this gene, encoding multiple isoforms. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: PrP, Histone, HAD, ACID, Atm
Papers on DIO-1
Dido mutations trigger perinatal death and generate brain abnormalities and behavioral alterations in surviving adult mice.
Martínez-A et al., Madrid, Spain. In Proc Natl Acad Sci U S A, May 2015
We recently proposed a role for Dido3, the main product of the death inducer-obliterator (dido) gene, in histone deacetylase 6 delivery to the primary cilium [Sánchez de Diego A, et al. (2014) Nat Commun 5:3500].
Proteomic characterization of human coronary thrombus in patients with ST-segment elevation acute myocardial infarction.
Barderas et al., Toledo, Spain. In J Proteomics, 2014
DIDO1 protein was found to correlate negatively with thrombus fibrin, and was found up-regulated in the plasma of these STEMI patients, which may constitute a starting point for further analyses in the search for biomarkers of thrombosis.
Identification and validation of genetic variants that influence transcription factor and cell signaling protein levels.
Jones et al., Chicago, United States. In Am J Hum Genet, 2014
Notably, we replicated and functionally validated a trans pQTL relationship between the KARS lysyl-tRNA synthetase locus and levels of the DIDO1 protein.
The death-inducer obliterator 1 (Dido1) gene regulates embryonic stem cell self-renewal.
Songyang et al., Guangzhou, China. In J Biol Chem, 2014
In this study, we report our findings that Dido1, a target of canonical transcription factors such as Oct4, Sox2, and Nanog, plays an important role in regulating ES cell maintenance.
Dido3-dependent HDAC6 targeting controls cilium size.
van Wely et al., Madrid, Spain. In Nat Commun, 2013
Here, we show that death inducer obliterator (Dido3)-dependent targeting of histone deacetylase 6 (HDAC6) is a key determinant of cilium size in growth-arrested cells.
Dido3 PHD modulates cell differentiation and division.
Kutateladze et al., Aurora, United States. In Cell Rep, 2013
Death Inducer Obliterator 3 (Dido3) is implicated in the maintenance of stem cell genomic stability and tumorigenesis.
Death inducer-obliterator 1 (Dido1) is a BMP target gene and promotes BMP-induced melanoma progression.
Bosserhoff et al., Regensburg, Germany. In Oncogene, 2013
We identified death inducer-obliterator 1 (Dido1) as a BMP-specific Smad-regulated target gene, which was confirmed by qRT-PCR, immunofluorescence staining and electrophoretic mobility shift assay experiments.
New targets for the antitumor activity of gambogic acid in hematologic malignancies.
Chen et al., Wuhan, China. In Acta Pharmacol Sin, 2013
These include the regulation of expression and intracellular positioning of nucleoporin and nucleophosmin; downregulation of steroid receptor coactivator-3 (SRC-3) and its downstream proteins; upregulation of death inducer-obliterator (DIO-1); downregulation of HERG potassium channel; as well as induction of reactive oxygen species (ROS) accumulation.
TPX2 and AURKA promote 20q amplicon-driven colorectal adenoma to carcinoma progression.
Meijer et al., Amsterdam, Netherlands. In Gut, 2012
RESULTS: TPX2, AURKA, CSE1L, DIDO1, HM13, TCFL5, SLC17A9, RBM39 and PRPF6 affected cell viability and/or anchorage-independent growth.
CSE1L, DIDO1 and RBM39 in colorectal adenoma to carcinoma progression.
Fijneman et al., Amsterdam, Netherlands. In Cell Oncol (dordr), 2012
CSE1L, DIDO1 and RBM39 are located on the 20q amplicon and affect processes such as cell viability and anchorage-independent growth in colorectal cancer.
Ablation of Dido3 compromises lineage commitment of stem cells in vitro and during early embryonic development.
Martínez-A et al., Madrid, Spain. In Cell Death Differ, 2012
loss of Dido3 expression compromises differentiation of embryonic stem cells in vitro and of epiblast cells in vivo, resulting in early embryonic death at around day 8.5 of gestation
Toward a comprehensive characterization of the phosphotyrosine proteome.
Pettersson et al., Uppsala, Sweden. In Cell Signal, 2011
Also, more than half of the novel pTyr proteins were localized to the nucleus, of which three (PBX2, TEAD1 and DIDO1) were classified as transcription factors and two (CENPC1 and MAD2L1) are associated with cell division control.
Chronic stress and impaired glutamate function elicit a depressive-like phenotype and common changes in gene expression in the mouse frontal cortex.
Del Rio et al., Pamplona, Spain. In Eur Neuropsychopharmacol, 2011
Specifically, a dowregulation in genes that promote cell proliferation (Anapc7), cell growth (CsnK1g1), cell survival (Hdac3), and inhibition of apoptosis (Dido1) was observed.
Synaptonemal complex assembly and H3K4Me3 demethylation determine DIDO3 localization in meiosis.
van Wely et al., Madrid, Spain. In Chromosoma, 2009
results indicate that histone H3 lysine 4 demethylation modulates DIDO3 localization in meiosis and suggest epigenetic regulation of the synaptonemal complex
[Mechanism of gambogic acid-induced apoptosis in Raji cells].
He et al., Wuhan, China. In Zhongguo Shi Yan Xue Ye Xue Za Zhi, 2009
Gambogic acid induces the apoptosis of Raji cells through DIO-1 upregulation, nuclear translocation, Bcl-xL downregulation and caspase 3 activation.
Gambogic acid induces death inducer-obliterator 1-mediated apoptosis in Jurkat T cells.
Wu et al., Wuhan, China. In Acta Pharmacol Sin, 2008
Gambogic acid induces DIDO1-mediated apoptosis in Jurkat T cells.
Dido disruption leads to centrosome amplification and mitotic checkpoint defects compromising chromosome stability.
Martínez-A et al., Madrid, Spain. In Proc Natl Acad Sci U S A, 2007
Dido3, the largest splice variant of the Dido gene, is a centrosome-associated protein whose disruption leads to supernumerary centrosomes, failure to maintain cellular mitotic arrest, and early degradation of the mitotic checkpoint protein BubR1.
Osteoblast apoptosis and bone turnover.
Stanislaus et al., Indianapolis, United States. In J Bone Miner Res, 2001
In reviewing selected work on interdigital apoptosis in the developing skeleton, we discuss the putative roles of the bone morphogenetic proteins (BMPs), Msx2, RAR-gamma, and death inducer obliterator 1 (DIO-1).
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